Airway hypoxia of the lung resulting from high altitude exposure and several cardiopulmonary diseases leads to pulmonary vascular constriction, pulmonary hypertension and sometimes, right heart failure. This response to hypoxia which occurs in humans and animals is not fully understood. This has been the impetus to develop and study animal models of hypoxic pulmonary hypertension. Through selective breeding we have developed a group of cattle that are susceptible and another group that are resistant to the development of hypoxic pulmonary hypertension. Efforts are also being made to develop a miniature swine model using a similar approach. Studies thus far in the cattle model have shown that the traits for susceptibility and resistance are transmitted from parents to offspring; susceptible cattle have thicker-walled and more reactive pulmonary vessels than the resistant cattle; susceptible cattle show a tendency to have a lower alveolar oxygen relative to the resistant animals which might indicate a blunted ventilatory response to hypoxia. Whether these traits are genetically transmitted from parent to offspring or are acquired, possible inutero remains to be determined. Proposed studies for next year include measurements of hypoxic and hypercapnic ventilatory drives and pulmonary vascular responses to hypoxia and other vasoactive agents, in susceptible and resistant calves starting within 72 hours after birth. The results of our studies could be important to both human and animal health. BIBLIOGRAPHIC REFERENCES: McMurtry, I .F., Weir, E. K., Reeves, J. T., Will, D. H. and Grover, R. F., 1976. Prostaglandin Synthesis Does Not Mediate the Pulmonary Vasodilatory Effect of Acetylcholine. Prostaglandins, 11:63-69. Jensen, R., Pierson, R., Braddy, P., Saari, D., Benitez, A., Horton, D., Lauerman, L., McChesney, A., Alexander, A., and Will, D. H. 1976. Brisket Disease in Yearling Feedlot Cattle. JAVMA, 169(5) :515-517.